Department of Medicine Faculty Profile

Kimm Hamann
Section of Pulmonary / Critical Care
Research Associate (Professor)

e-mail: khamann@medicine.bsd.uchicago.edu

Training:

Degree	Year	Institution	Area
BA	1976	Augustana College	Biology
MS	1978	University of Minnesota	Zoology
PhD	1986	University of Minnesota	Zoology
Fellowship	1988	Mayo Clinic	Immunology

Academic Interests:

Dr. Hamann’s research focuses primarily on the role of the TNF family death receptors, particularly Fas/CD95 receptor, in hematopoiesis and inflammation, and on mitochondrial pathways of cell death in ischemia/reperfusion injury of cardiomyocytes. He is investigating "non-apoptotic" Fas signaling, including activation of NF-kB, and the role of its gene targets in apoptosis of inflammatory cells. In cardiomyocytes, he is studying mechanisms of apoptosis and "preconditioning"-induced protection against apoptosis, including NF-kB-mediated events, and involvement of protective molecules.

Representative Publications:

Hamann KJ, JE Viera, AJ Halayko, D Dorscheid, SR White, SM Forsythe, B Camoretti-Mercado, KF Rabe and J Solway. Fas (CD95) crosslinking induces apoptosis in human airway smooth muscle cells. Am J Physiol 278:L618-624, 2000.
Qin Y, B Camoretti-Mercado, L Blokh, CG Long,FD Ko and KJ Hamann. Fas resistance of leukemic eosinophils is due to activation of NF-kB by Fas ligation. J Immunol 169:3536-3544, 2002.
Qin Y, TL Vanden Hoek, K Wojcik, CQ Li, ZH Shao, T Anderson, LB Becker and KJ Hamann. Reperfusion, not simulated ischemia, initiates intrinsic apoptosis injury in cardiomyocytes. Am J Physiol 284:H141-H150, 2003.
Abella BS, D Zhao, J Alvarado, K Hamann, TL Vanden Hoek, LB Becker. Intra-Arrest cooling improves outcomes in a murine cardiac arrest model. Circulation 109:2786-2791, 2004.
Qin Y, T Vanden Hoek, K Wojcik, CQ Li, ZH Shao, T Anderson, and KJ Hamann. Caspase-dependent cytochrome c release in reperfusion-induced apoptosis of ischemic chick cardiomyocytes Amer. J. Physiol. (Heart Circ Physiol) 286:H2280-H2286, 2004.